ENG and hereditary hemorrhagic telangiectasia: Because haploinsufficiency is the mechanism underlying HHT [2], and the (c.-58 G > A) in Endoglin promoter seemed to reduce, at least in vitro, the promoter activity in a reporter (Fig. 2), we decided to assess activated monocytes from 1 HHT patient and his healthy brother, evaluating Endoglin expression in both patients side by side.